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Transactivation of Vimentin by ß-Catenin in Human Breast Cancer Cells¹

Laboratory of Tumor and Developmental Biology, University of Liège, CHU Sart-Tilman, B23, B-4000 Liège, Belgium [C. G., M. M., P. R., J-M. F.], and Unité INSERM U.514, Laboratoire Pol Bouin, IFR 53, CHU Maison Blanche, Reims, France [M. P., B. N-R., P. B.]

The cytoplasmic and nuclear redistribution of ß-catenin and the de novo expression of vimentin are frequently involved in the epithelial-to-mesenchymal transition associated with increased invasive/migratory properties of epithelial cells. Because ß-catenin can act as a coactivator of transcription through its binding to the T-cell factor (TCF)/lymphoid enhancer factor 1 transcription factor family, we have explored the possibility that ß-catenin/TCF could directly transactivate vimentin. We first compared vimentin expression in relation with the localization of ß-catenin in eight breast cancer cell lines displaying various degrees of invasiveness and in a model of cell migration using human mammary MCF10A cells. We could thus show a cytoplasmic and/or nuclear distribution of ß-catenin in invasive/migratory cells expressing vimentin, but not in noninvasive/stationary vimentin-negative cell lines. In addition, the human vimentin promoter was found to be up-regulated by ß-catenin and TCF-4 cotransfection. Varying with the cellular background, a diminution of this up-regulation was observed when the putative ß-catenin/TCF binding site of the vimentin promoter was mutated. Our results therefore demonstrate that the vimentin promoter is a target of the ß-catenin/TCF pathway and strongly suggest an implication of this regulation in epithelial cell migration/invasion.

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